Tanneau R S, Henry A, Rouhart F, Bourbigot B, Garo B, Mocquard Y, Goas J Y
Renal and Critical Care Unit, University Hospital, Brest, France.
J Clin Psychiatry. 1994 Aug;55(8):349-54.
Patients with self-induced water intoxication usually tolerate a large, rapid increase in plasma sodium without developing osmotically induced central pontine myelinolysis. However, we have previously reported a case of clinically suspected pontine myelinolysis in a patient with self-induced water intoxication. The purpose of our study was to investigate if a subgroup of these patients may also be vulnerable to neurologic complications of hyponatremia therapy.
Over a 10-year period, we identified retrospectively 12 polydipsic patients having a total of 24 episodes of symptomatic hyponatremia with plasma sodium < or = 115 mmol/L. The mode of treatment, the kinetics of correction, and the neurologic outcome were recorded. The presence of alcoholism was noted.
Seven patients recovered uneventfully from 19 episodes of symptomatic hyponatremia. Five patients had delayed neurologic complications. Late therapy and/or respiratory arrest might have been associated with the complications for 2 patients. The other 3 patients experienced clinical features of central pontine myelinolysis leading to death in 1. Patients with neurologic complications had a higher maximal 24-hour increase in plasma sodium concentration (21.8 +/- 3.9 vs. 15.5 +/- 5.1 mmol/L, p < .02), and a higher incidence of both overcorrection to hypernatremia and chronic alcoholism, often associated with poor nutrition. All 5 patients became water intoxicated at home, and 2 patients with pontine dysfunction had subacute rather than acute hyponatremia.
A large rapid increase in plasma sodium may also be detrimental in patients with self-induced water intoxication when they are alcoholic, malnourished, and have nonacute hyponatremia.
自我诱导性水中毒患者通常能耐受血浆钠浓度大幅快速升高,而不发生渗透性诱导的中枢性桥脑髓鞘溶解症。然而,我们之前曾报道过一例临床疑似桥脑髓鞘溶解症的自我诱导性水中毒患者。我们研究的目的是调查这些患者中的一个亚组是否也易患低钠血症治疗的神经系统并发症。
在10年期间,我们回顾性地确定了12例烦渴患者,他们共有24次有症状的低钠血症发作,血浆钠浓度≤115 mmol/L。记录治疗方式、纠正动力学和神经学结果。记录是否存在酒精中毒。
7例患者从19次有症状的低钠血症发作中顺利康复。5例患者出现延迟性神经系统并发症。2例患者的并发症可能与延迟治疗和/或呼吸骤停有关。另外3例患者出现中枢性桥脑髓鞘溶解症的临床特征,其中1例死亡。出现神经系统并发症的患者血浆钠浓度24小时最大升高幅度更高(21.8±3.9 vs. 15.5±5.1 mmol/L,p<.02),高钠血症过度纠正和慢性酒精中毒的发生率更高,且常伴有营养不良。所有5例患者在家中发生水中毒,2例桥脑功能障碍患者为亚急性而非急性低钠血症。
对于患有酒精中毒、营养不良且为非急性低钠血症的自我诱导性水中毒患者,血浆钠浓度大幅快速升高也可能有害。